Differential tissue expression of erythroblast macrophage protein in a MRL/lpr mouse model of lupus

Lupus ◽  
2019 ◽  
Vol 28 (7) ◽  
pp. 843-853
Author(s):  
H Fan ◽  
N Li ◽  
P Fan ◽  
X Hu ◽  
K Liang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mouse Model ◽  
Mrna Expression ◽  
Lupus Erythematosus ◽  
Tissue Expression ◽  
Expression Rate ◽  
Macrophage Protein ◽  
And Control ◽  
Liver Tissues ◽  
Brain Tissues

Objective The objective of this study was to observe the expression features of erythroblast macrophage protein (EMP) between the tissues of MRL/lpr mice, a mouse model of systemic lupus erythematosus (SLE), and control mice. Methods We examined the serum ANA in both mice groups through indirect immunofluorescence (IIF). Expression features of EMP in bone marrow, liver, renal, spleen, brain, and lung tissues of the MRL/lpr mice and control mice groups were followed using quantitative real-time polymerase chain reaction (Q-PCR). Meanwhile, the expression of EMP was located through immunohistochemical (IHC) studies and the expressive cell identified through double immunofluorescent labeling. Results IIF showed that lupus mice have strong positive fluorescence, but no significant fluorescence was observed in control mice. Q-PCR detection revealed that EMP was expressed in the marrow, liver, renal, spleen, lung, and brain tissues of lupus mice. The highest levels were observed in the bone marrow, but there was no statistical difference between these tissues. EMP mRNA expression in the liver ( t = 2.747, p = 0.01) and bone marrow ( t = 3.853, p = 0.008) of lupus mice was significantly higher than in the control mice. However, no differences in EMP mRNA expression were observed in the renal, spleen, lung, and brain tissues between the lupus and control mice ( p > 0.05). In addition, the IHC results showed that EMP protein is ubiquitously expressed in all of the tissues of the lupus and control mice. The positive expression rate in the bone marrow and liver tissues of the lupus mice was higher than in the control mice, but without an obvious difference in the other tissues. The double IF staining method shows that EMP protein was expressed in macrophages in the tissues of the lupus mice and the control mice. Conclusions Our data showed that EMP is ubiquitously expressed in macrophages at all of the tissues of the lupus and control mice. However, the expression of EMP in bone marrow and liver tissues of lupus mice was higher than in the control mice, which indicates that EMP may be important in the development of SLE.

scholarly journals An integrated analysis of lncRNA and mRNA expression profiles in the kidneys of mice with lupus nephritis

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e10668
Author(s):  
Juan Wang ◽  
Xiongfei Wu ◽  
Yafang Tu ◽  
Jianzhong Dang ◽  
Zhitao Cai ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Mrna Expression ◽  
Lupus Erythematosus ◽  
Expression Profiles ◽  
Inflammatory Factors ◽  
Integrated Analysis ◽  
Limited Information ◽  
Rna Seq ◽  
And Control ◽  
Upregulated Genes

Long noncoding RNAs (lncRNAs) are persistently expressed and have been described as potential biomarkers and therapeutic targets in various diseases. However, there is limited information regarding lncRNA expression in the tissue of kidney exhibiting lupus nephritis (LN)a serious complication of systemic lupus erythematosus (SLE). In this study, RNA sequencing (RNA-seq) was performed to characterize the lncRNA and mRNA expression in kidney tissues from LN (MRL/lpr) and control mice. We identified 12,979 novel lncRNAs in mouse. The expression profiles of both mRNAs and lncRNAs were differed significantly between LN and control mice. In particular, there were more upregulated lncRNAs and mRNAs than downregulated ones in the kidney tissues of LN mice. However, GO analysis showed that more downregulated genes were enriched in immune and inflammatory response-associated pathways. KEGG analysis showed that both downregulated and upregulated genes were enriched in a number of pathways, including the SLE pathway, and approximately half of these SLE-associated genes encoded inflammatory factors. Moreover, we observed that 2,181 DElncRNAs may have targeted and regulated the expression of 778 mRNAs in LN kidney tissues. The results of this study showed that 11 DElncRNAs targeted and were co-expressed with six immune and SLE-associated genes. qPCR analysis confirmed that lncRNA Gm20513 positively regulated the expression of the SLE-associated gene H2-Aa. In conclusion, the results of our study demonstrates that lncRNAs influence the progression of LN and provide some cues for further study of lncRNAs in LN. These results regarding the lncRNA-mRNAregulatory network may have important value in LN diagnosis and therapy.

scholarly journals Mitochondrial tRNA in hyperthyroidism.

1995 ◽  
Vol 42 (2) ◽  
pp. 227-231
Author(s):  
K Pasternak ◽  
S Szymonik-Lesiuk ◽  
H Brzuszkiewicz-Zarnowska ◽  
T Borkowski
Keyword(s):  
Amino Acids ◽  
Brain Mitochondria ◽  
Mitochondrial Trna ◽  
And Control ◽  
The Brain ◽  
Liver Tissues ◽  
Brain Tissues

The mitochondrial tRNA were prepared from liver and brain tissues of thyroxinized and control rabbits. The presence of tRNA for twenty amino acids both in liver and brain mitochondria was revealed. The quantity of radioactive amino acids bound to the mitochondrial tRNA was higher in hyperthyreosis than in control animals but considerable differences between the brain and liver tissues were observed.

scholarly journals Differential Oncogene and TNF-α mRNA Expression in Bone Marrow Cells from Systemic Lupus Erythematosus Patients

1998 ◽  
Vol 48 (5) ◽  
pp. 551-556 ◽  
Author(s):  
ALVARADO-DE LA BARRERA ◽  
ALCOCER-VARELA ◽  
RICHAUD-PATIN ◽  
ALARCÓN-SEGOVIA ◽  
LLORENTE
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Bone Marrow ◽  
Mrna Expression ◽  
Lupus Erythematosus ◽  
Bone Marrow Cells ◽  
Systemic Lupus ◽  
Tnf Α ◽  
Marrow Cells

scholarly journals Blood pressure in a hypertensive mouse model of SLE is not salt-sensitive

2011 ◽  
Vol 301 (5) ◽  
pp. R1281-R1285 ◽  
Author(s):  
Keisa W. Mathis ◽  
Marcia Venegas-Pont ◽  
Chester W. Masterson ◽  
Katie L. Wasson ◽  
Michael J. Ryan
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Mouse Model ◽  
Disease Activity ◽  
Lupus Erythematosus ◽  
Normal Diet ◽  
Renal Inflammation ◽  
Salt Sensitive Hypertension ◽  
And Control ◽  
And Oxidative Stress

Systemic lupus erythematosus (SLE) is a risk factor for hypertension. Previously, we demonstrated that an established mouse model of SLE (female NZBWF1 mice) develops hypertension with renal inflammation and oxidative stress, both characteristics known as contributing mechanisms to the development of salt-sensitive hypertension. On the basis of this model, we hypothesized that blood pressure in SLE mice would be salt-sensitive. Thirty-week-old female SLE and control mice (NZW/LacJ) were fed 8% high-salt (HS) diet or normal diet (0.4% salt) for 4 wk. Plasma levels of double-stranded DNA (dsDNA) autoantibodies, a marker of SLE disease activity, were increased in SLE mice compared with controls (472 ± 148 vs. 57 ± 17 U/ml × 1,000, P < 0.001). HS did not alter dsDNA autoantibody levels in SLE or control mice. Mean arterial pressure was increased in SLE mice compared with controls (132 ± 3 vs. 118 ± 2 mmHg, P < 0.001) and was not significantly altered by the HS diet in either group. Similarly, albuminuria was higher in SLE mice compared with controls (10.7 ± 9.0 vs. 0.3 ± 0.1 mg/day) but was not significantly increased in SLE or control mice fed a HS diet. In summary, blood pressure during SLE is not salt-sensitive, and the HS diet did not adversely affect SLE disease activity or significantly augment albuminuria. These data suggest that renal inflammation and oxidative stress, characteristics common to both SLE and models of salt-sensitive hypertension, may have diverging mechanistic roles in the development of hypertension.

scholarly journals High-trans fatty acid and high-sugar diets can cause mice with non-alcoholic steatohepatitis with liver fibrosis and potential pathogenesis

2020 ◽  
Author(s):  
Xin Xin ◽  
Bei-yu Cai ◽  
Cheng Chen ◽  
Hua-jie Tian ◽  
Xin Wang ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Mouse Model ◽  
Mrna Expression ◽  
Signaling Pathways ◽  
Model Group ◽  
Expression Levels ◽  
Alcoholic Steatohepatitis ◽  
Tgf Β1 ◽  
Mrna Expression Levels ◽  
Liver Tissues

Abstract Aims To establish a mouse model of non-alcoholic steatohepatitis (NASH) within liver fibrosis using a high-fat and high-carbohydrate diet (HFHC) and to analyze potential pathogenesis using a transcriptome microarray. Methods Sixty mice were stratified by weight and randomly divided into HFHC model and control (Con) groups, with 30 mice in each group. Both HFHC and Con mice were euthanized at 0, 20 and 30 weeks. The following analyses were performed: biochemical analysis; histological assessment; Col-I, α-SMA and TGF-β1 protein and mRNA expression levels; and transcriptomic gene chip analysis. Results Compared with the Con group at each time point, the body weight and liver wet weight of the HFHC model group mice were significantly higher. At 30 weeks, ALT, AST, FBG and FINS levels or activities and TG and HYP contents in the HFHC model group were significantly elevated. Severe steatosis was present in the liver tissues from HFHC group mice. Substantial perisinusoidal fibrosis with a cage-like structure and bridging formations were observed in the liver. Col-I, α-SMA and TGF-β1 protein and mRNA expression levels in liver tissues from HFHC mice increased over time. Compared with the Con group, the HFHC group had 151 differentially expressed genes that were involved in 41 signaling pathways. Conclusions After 30 weeks of a HFHC diet, the mice exhibited substantial liver fibrosis, hepatic steatosis, ballooning degeneration and inflammation. The formation of an experimental NASH combined with liver fibrosis mouse model may be related to ECM-receptor interaction, Toll-like receptor signaling and other signaling pathways.

Establishment of a Mouse Model of Aplastic Anemia Complicated By Iron Overload

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4555-4555
Author(s):  
Dijiong Wu ◽  
Xiaowen Wen ◽  
Baodong Ye ◽  
Wenbin Liu ◽  
Yanting Gao ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mouse Model ◽  
Iron Overload ◽  
Western Blot ◽  
Aplastic Anemia ◽  
Mrna Expression ◽  
Serum Iron ◽  
Composite Model ◽  
Expression Levels ◽  
Mrna Expression Levels

Abstract Aplastic anemia (AA) is a common hematologic disease characterized by hematopoietic failure of the bone marrow and pancytopenia of the peripheral blood. Some patients with AA suffer from transfusion-induced iron overload secondary to long-term blood transfusions due to moderate and severe anemia. Topics related to iron overload and chelation therapy have recently become important in hematologic diseases, especially in hematopoietic failure. However, no animal model of AA complicated by iron overload has been developed, which affects drug research and development. The purpose of our study is to establish a mouse model of aplastic anemia complicated by iron overload. We firstly controlled the total dose of iron supplements (2.0 *103 mg/kg) and compared how serum iron and ferritin levels varied among different dosage regimens to determine the best dosage and duration for the development of an iron overload model in mice (we finally chose the 200 mg/w/kg * 10 weeks). A composite model of AA was successfully established on the principle of immune-mediated bone marrow failure: DBA/2 mice were euthanized by cervical dislocation and the thymuses were taken out using aseptic techniques for the preparation of cell suspensions of 5 * 106/mL; Balb/c mouse were given whole-body irradiation with 60Co 6.0 Gy at 1 Gy/min, after which 0.2 mL of the prepared cell suspensions was injected into each mouse via the caudal vein within 4 h. We then compared the differences in liver volume, peripheral hemogram, bone marrow pathology, serum iron, serum ferritin, pathological iron deposition in multiple organs (liver, bone marrow, spleen), liver hepcidin, bone morphogenetic protein 6 (BMP6), SMAD family member 4 (SMAD4), transferrin receptor 2 (TfR2) protein, and mRNA expression levels among the Normal Control, AA, Iron Overload, and Composite Model groups to validate the composite model and to explore the pathogenesis and features of iron overload in the composite model. The results indicated significant abnormalities in iron metabolism parameters in mice with AA, which was reflected in the significant decrease of hepcidin expression in the liver (P < 0.01) that basically paralleled the changes in BMP6, SMAD4, and TfR2. Iron Overload Group had a suppressed hepcidin, BMP6, and SMAD4 mRNA expressions in liver, but these parameters were higher than in the AA group (P < 0.01). Association with iron overload would not further downregulate the negative parameters of iron deposition in mice with AA, and SMAD4 and TfR2 protein levels and hepcidin and SMAD4 mRNA expression levels were lower in the AA group than in the Composite Model group (P < 0.01 or P < 0.05). (see Fig.1 and Fig.2) The established model is basically consistent with the clinical manifestations and pathogenesis of AA complicated by transfusion-induced iron overload. This successful establishment will help in the screening of iron chelation drugs and studies on pharmacological mechanisms. Figure 1. Western-blot a nalysis of hepcidin, BMP6, SMAD4 and TfR2 expression among groups Figure 1. Western-blot a nalysis of hepcidin, BMP6, SMAD4 and TfR2 expression among groups Figure 2. Analysis of hepcidin, BMP6, SMAD4 and TfR2 mRNA expression levels among different groups Figure 2. Analysis of hepcidin, BMP6, SMAD4 and TfR2 mRNA expression levels among different groups Disclosures No relevant conflicts of interest to declare.

Investigation of the Association Between Carotid Artery Intima-Media Thickness (IMT) and Cardiac Risk Factors in Patients with Systemic Lupus Erythematosus

2020 ◽  
Vol 16 (2) ◽  
pp. 125-133
Author(s):  
Zahra Rezaieyazdi ◽  
Sima Sedighi ◽  
Masoumeh Salari ◽  
Mohammadreza H. Fard ◽  
Mahmoud R. Azarpazhooh ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Lupus Erythematosus ◽  
Serum Insulin ◽  
Venous Blood ◽  
Test Group ◽  
Control Groups ◽  
Significant Difference ◽  
The Mean ◽  
And Control

Background: The relationship between SLE and traditional risk factors for cardiovascular events was evaluated. Methods: The data regarding sixty patients with SLE and 30 healthy controls (age and sex matched) were gathered using SLEDAI forms. Venous blood (10mL) from all the participants was examined for hs-CRP, homocysteine, VCAM1, CBC, anti-DNA antibody, C3, C4, low-density lipoprotein (LDL), cholesterol, FBS and triglyceride. : The IMT of carotid arteries was determined bilaterally by ultrasound. Other measurements included insulin levels via Elisa (Linco/Millipore Corp) and the HOMA-IR index for insulin resistance. Results: The mean age (in years) in the test and control groups was 28.8±10.3 (18-52) and 33.8±9.13 (18-48), respectively. Results: The mean age (in years) in the test and control groups was 28.8±10.3 (18-52) and 33.8±9.13 (18-48), respectively. : The average IMT in the test group was directly related to serum levels of VCAM1 (p<0.001), homocysteine (p<0.001), cholesterol (p<0.009), LDL (p<0.001), TG (p<0.001), and FPG (p=0.004). The association between other risk factors, insulin resistance, carotid IMT and SLEDAI, was nonexistent. Mean insulin and insulin resistance levels in all the participants were 0.43±2.06 µU/mL and 0.09±0.44, respectively. There was no significant difference between the test and control groups regarding serum insulin and insulin resistance levels (p=0.42 and p=0.9, respectively). None of the risk factors, such as hsCRP, VCAM1, or homocysteine, were shown to be related to insulin resistance (p=0.6, p=0.6, p=0.09, respectively). Conclusion:: Our findings did not show an increase in the prevalence of atherosclerosis in patients with SLE. There was no association between IMT and insulin resistance. However, the former was associated with FPG, total cholesterol, LDL, TG, homocystein and VCAM1.

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